Related Experiment Video
Updated: Aug 23, 2026
Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
Published on: June 26, 2018
Carvedilol differentially regulates cytokine production from activated human peripheral blood mononuclear cells
Shih-Ping Yang1, Ling-Jun Ho, Shu-Meng Cheng
1Cardiology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China.
Insights
Carvedilol, a cardio-protective drug, differentially regulates immune cell cytokine production. It inhibits interferon-gamma (IFN-gamma) while enhancing interleukin-12 (IL-12), potentially impacting atherosclerosis development.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Pharmacology
Background:
- Chronic inflammation is a key factor in atherosclerosis.
- Activated monocytes and their cytokines significantly contribute to this inflammation.
Purpose of the Study:
- To investigate the effects of carvedilol on cytokine production in human immune cells.
- To understand how carvedilol modulates inflammatory responses relevant to cardiovascular disease.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure cytokine levels.
- Human peripheral blood mononuclear cells (PBMCs), purified monocytes, and activated macrophages were stimulated with various agents.
- The impact of carvedilol on cytokine production (IFN-gamma, IL-12, TNF-alpha, IL-10) was analyzed.
Main Results:
- Carvedilol inhibited interferon-gamma (IFN-gamma) production in PHA- and ConA-stimulated PBMCs.
- Interleukin-12 (IL-12) production was enhanced by carvedilol in PBMCs, purified monocytes, and activated macrophages.
- Tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) production showed marginal or no significant changes.
Conclusions:
- Carvedilol differentially regulates cytokine production in immune cells, notably up-regulating IL-12.
- These immunomodulatory effects suggest a potential mechanism for carvedilol's therapeutic benefits in cardiovascular conditions like atherosclerosis.
Abstract:
Chronic inflammation is one of the important mechanisms involved in atherosclerosis formation. The activated monocytes and their secreted cytokines contribute significantly to this inflammatory process. Here we examined the effects of carvedilol, a recently introduced cardio-protective alpha-1- and beta-receptor blocker, on cytokine production from various stimuli-activated human immune effector cells. By ELISA analysis, we showed that carvedilol inhibited interferon-gamma (IFN-gamma), but enhanced interleukin (IL)-12 production in phytohemagglutinin (PHA)- and concanavalin A (ConA)-stimulated human peripheral blood mononuclear cells (PBMCs). The production of tumor necrosis factor-alpha (TNF-alpha) was marginally affected. When purified monocytes were examined, we observed the consistent up-regulation of IL-12 production while both IL-10 and TNF-alpha were unaffected or marginally down-regulated, respectively, by carvedilol. In agreement with the observation in monocytes, the production of IL-12 from activated macrophages was also up-regulated by carvedilol. We concluded that carvedilol might mediate its therapeutic effects through differentially regulating cytokine production from activated mononuclear cells, including at least monocytes and macrophages.
